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68 Cards in this Set
- Front
- Back
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Normal circulation-
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- VC--->RA--->tricuspid V--->RV---> pulm. V--->PA---> lungs
--->LA--->bicuspid/mitral V--->LV--->Aortic V--->Aorta |
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Layers of the heart-
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- Pericardium- often fibrous layer- elastin + collagen
-Mesothelium- parietal layer- fluid on both sides- lube - Epicardium- visceral pericardium- elastin rich - (Coronary art. between) - Myocardium- BV++, cap. parallel to sheets of myocytes - Endocardium- continuous c tunica intima of BV -Endocardium |
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The heart-
Atrial myocytes- Heart valves- Purkinje fibres- Heart wall thickness |
- Situated in the mediastinum
- Atrial cardiac myocytes produce atrial natriuretic factor- controls BP---> Dec Na+ absorpt.= dec blood vol. - Heart valves- - Lined by endocardium - Have dense CT + elastin + spongiosa of loose CT - Atrioventric. valves tethered by chordae tenineae to papillary mm of ventricles - Purkinje fibres contained in endocardium - LV wall+ interV septum=2-4x thickness of RV free wall |
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Embryonic remnants-
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- Foramen ovale- between atria- bypasses lungs
- Ductus arteriosus- between Aorta + PA- bypasses lungs - Ductus venosus- Between umbilical vein +VC- bypasses liver and hepatic portal vein. |
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Terminology-
Preload- Afterload- |
Preload- the initial stretching of the cardiac myocytes prior to contraction
Afterload- press. that heart chambers must generate in order to eject blood |
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Congenital pathologies of the heart
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- Abnormal dev. vs. Persistence of foetal structures
- Patent DA- - Atrial septal defect- - Ventricular septal defect- - Atrioventricular septal defect |
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Patent DA
Normal- Abnormal- Breeds- |
-Normal
- Prominent sm mm layer sensitive to stim by chemical factors after birth- eg. Adren., N.A, angiotensin, o2, ACh. - After closure---> fibrous Ligamentum arteriosum - >5 days= abnormal, but may be patent to probing for few weeks - Failure- hypoplasia/ abnormal distrib. of sm mm - Breeds- Bichon Frise, GSD |
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Consequences of PDA
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- Depend on size of DA and pressure difference between pulm and systm circ.
- (If systemic press.>Pulmonary) - L--->R shunt (A--->PA) - Presents as continuous "machinary murmur" - Compensatory hypertrophy of L and R V - (Inc pulm flow---> Inc return to LA and V--->Inc preload (vol. overload) - L overload---> LA dilation + eccentric hyperT of LV - Exposure to systm BP + Inc P. BV---> RV overload - RV overload (afterload) ---> concentric hyperT of RV - May be dil. of ascend. aorta + PA (Inc press. + turb.) - May predisp to thombosis - If Pulm hypertens. occurs---> Pulm>Systemic - Reversal of shunt (R--->L) ---> cyanosis and hypoxia -OR - Blood only shunted L--->R during systole |
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Atrial septal defect
Define- Normal- Breeds- Consequences- |
- Incomplete closure of foetal foramen ovale
- Defect in oval fossa - Funct. closure soon after birth/ anatom.= days-weeks - Slower in ruminants- patent to probing 2-3 weeks - Breeds- Boxers and Doberman - Consequences- - Small defect may be fine - Allows L---> R shunt - No mumor as A pressure diff. is small - Larger defect- - L--->R shunt --->RV vol overload (inc preload)---> eccentric dilation and hypertrophy ---> Relative pulm. stenosis---> "flow murmor" - Compensatory dilation of A - If severe pulm. hypertension--> R-->L shunt---> hypoxia |
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Ventricular septal defect-
Define- Types- Breeds- Consequences- |
- Often a single defect, but can be multiple
- Perimembranous- involves membrane and mm - VS - Muscular- mm only - Breeds- English bulldog, springer, beagle - Consequences- Dep. on size, location and relative pulm + systm pressures -Small defect- no signif.- poss. spont. closure in dogs - Large defect- eq. of pressure between V - L--->R shunt - Inc BP +B vol. (pre +afterload)---> L+R V hypertrophy - If Pulm hypertension- shunt may reverse |
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Atrioventricular septal defect-
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- Aka- endocardial cushion defect/ AV canal defect
- Consequences- - Hole in septum---> incomp. seperation of L + R A and V - Single AV valve formation (due to lack of L+R sep.) ---> mixing of systm and pulm blood - Pulm art exposed to inc. press. + vol--->pulm hypertens ---> Change in vasc---> Inc hypertens. ---> Prob. with blood supply due to inc. resistance |
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Developmental pathologies of valves-
(x7) |
- Pulmonic stenosis
- Valvular - Subvalvular - Supravalvular - Pulmonic atresia - Aortic/ subaortic stenosis - Valvular - Subvalvular - Mitral dysplasia - Tricuspid dysplasia - Tricuspid atresia - Vavular haematomas - Haematocysts - Lymphocysts |
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Pulmonic valve
Types- Consequences- |
-Pulmonic stenosis
- Valvular- caused by valve dysplasia- - Inc resist.---> thickening - Small - Fused - Subvalvular- due to subvalv. fibrous rings - Supervalv.- due to narrowing of PA - Consequences- - Inc resist. for BF---> Inc RV afterload---> hypertrophy - Pulmonic atresia- lack of valve formation |
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Aortic valve
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- Stenosis- most commonly subaortic subvalv.
- Excess tissue- appears as plaques/ band of endocardial CT, may adhere to valves - May be progressive - Consequences- - Inc resist. through valve---> Inc afterload---> inc press. ---> Concentric hypertrophy of LV - Turbulence through aorta---> dilation |
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AV valves-
Mitral- Tricuspid- |
- Dysplasias-
- Mitral valve- - Leaflets appear shortened and thickened - Chordae tendinae either short+ thick---> limit movement OR long and thin--->prolapse - Tricuspid valve- - Maldevelop. of valve, chord. tend. +/- papill. mm. |
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Consequences of AV valve dysplasia
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- Consequences of dysplasia-
- Stenosis- (A dilation) - Inc A blood vol.--->Inc A press.---> A hypertrop. and dilat. ( --->fibrillation) ---> Dec. V fill---> "backing up"---> Inc Pulm Resist.---> R sided hypertrophy ---> Inc venous congest + press. ---> stasis + thrombosis. - Insufficiency- (V eccentric hypertrophy) ---> Regurgitation ---> A and V dilation - Both |
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Tricuspid atresia
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- Lack of communication between RA and RV
- Can only survive if also have septal defects |
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Vascular haematomas
Define- Spp.- Significance- |
- Haematocysts and lymphocysts
- Blood/ lymph filled structures on the valves - Seen in calves - Probably no funct. significance. |
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Congenital abnormalities of BV
(x4) |
- Vascular rings-
- Persistent R aortic arch- Aorta on R not L ---> Ring formed c Aort., PA and Lig. art.- encircles oes/trach. - Transpositions- Aort + PA- req septal defects to survive - Partial transp.- PA and aort. from RV - Overriding/ dextroposition of aort---> bld from both V - Overriding PA---> PA overlies V septum, aort. from RV - Common art. trunk-Single art. trunk supplies systm, Pulm and coronary blood supply. - Anomolous pulm. venous connections |
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Other congenital heart conditions-
(x5) |
- Ectopia cordis- Heart not in thorax
- Divided RA (cor triatrium dexter) - Endocarial fibroelastosis - Tetralogy of Fallot 1) V. septal defect 2) Pulm. stenosis 3) RV hypertrophy 4) Dextroposition of aorta ---> Dec Pulm. BF + L-->R shunt ---> Cyanosis - Excessive moderator bands in LV of cat (- Normal in RV- prevents excessive dilation) |
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Pericardial dz
Fluid accum. (x4) |
- Fluid accum.-
- Hydropericardium- accum of serous transudate -2o to dz, inflam, neoplasia - Haemopericadium- can be due to rupture or puncture - Haemorrhagic pericardial effusion- idiopathic - Cardiac tamponade- compress. of heart---> Dec VR and filling---> Dec C.O.---> hypotension |
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Inflammatory pericardial dz
(x3) |
- Inflammatory pericarditis-
- Fibrinous- 2o to other dz- fibrinous inflam exudate - Suppurative- fibrinopurul. exudate accum. in sac - Constrictive - end stage of both above - Pus may fill sac + prevent dilation---> heart failure - Organising of granulation tissue |
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Other pericardial conditions-
(x2) |
- Metabolic changes-
- Serous atrophy of pericardal fat during starvation. - May have concurrent myocard. atrophy -Haemorrhage- Many causes- - eg- Septicaemia, mulb. heart dz, electrocution, agonal |
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Inflammatory endocardial dz
(x3) Describe- Cause- Gross- Micro- Pathology- |
- Valvular endocarditis-
- mitral and aortic most commom - Predisp. by turb BF - Caused by bacteria eg Strep, Arcanob., Erysipelothrix - Gross- Rough, vegetative lesions - Micro- look like thrombus on valve - Layers of fibrin and blood c bact. colonies overlying base layer of granulation tiss + inflam cells - Pathology- - Valvular stenosis or insufficiency - Septic emboli (R---> lungs, L---> Kidneys) - Mural endocarditis- After "blackleg" - Ulcerative endocarditis- Rare- often L. Atrium - Due to uraemia resulting from renal failure. |
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Degenerative endocardial dz-
(x2) |
- Valvular endocardosis
- Endocardial fibrosis and mineralisation |
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Valvular endocardosis-
Aka- Describe- Gross- Micro- Path- |
- Valvular endocardiOSIS
- Aka- myxomatous valvular heart dz/ chronic degen. valvular dz (CDVD) - Common in dogs (CKCS)= 75% heart failure - Slowly progressive - Usually mitral but can be tricuspid - Gross- - Smooth lesions c opaque, white nodular thickening - Micro- - Fibroblast prolif. + abundant mucopolysach. depos. - Patho- - Lax Chord. Tend.---> Valv. insuff---> regurg.---> Dec CO - Dilation and eccentric hypertrophy of A and V - Atrial mural thrombus -Jet lesions |
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Endocardial fibrosis-
Endocardial mineralisation- Subendothelial changes- Myocardial changes- |
- Endocardial lesions
- Multiple causes - fibrosis - After ulcerative endocarditis ( -renal failure) - Due to jet lesions - Diffuse fibrosis following prolonged dilation - Mineralisation - Vit D toxicity - Vit D analogues - Calciferol - Subendothelial mineralisation - Johnes dz - Senile changes - Myocardial - white speckled changes due to barbiturate ppt |
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Circulatory disturbances-
(x2) |
- Atrial thrombosis-
- Due to- - Dec BF in dilated atria - Hypertrophic cardiomyopathy (Cats) - Haemorrhage |
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Myocardial growth disturbances
Hypertrophy- 1o vs. 2o Types- |
- Primary- idiopathic, irreversible
- Due to hypertrophic cardiomyopathy - Secondary- causes - Inc. functional demand (Inc mech stim) - Inc hormonal demand - Hyperthyroidism- Inc synth of contract. prot. - Gross- Inc. mm mass present - Micro- Enlarged myocytes- plump or elongated - Types- - Concentric - Thickened walls (to gen. inc systolic press. req.) - Smaller/same size chamber - Eccentric - Thinner/same walls, dilated chamber due to inc B vol - May occur after concentric hypertrophy |
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Examples of cardiac hypertrophy-
RV- (x3) LV- (x3) Bilateral- (x3) |
- RV-
- Pulm. stenosis - Pulm. hypertension - Valvular insuff. - LV- - Aortic valve stenosis - Systm hypertension - Valv. insuff. - Bilateral- - V septal defects - Thyrotoxicosis - Hypertrophic cardiomyopathy |
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Maladaptive problems assoc with hypertrophy-
(x3) Myocardial atrophy Cause- |
- Chronic over-exposure of neuroendocrine stimuli
---> - Dec. Compliance ---> dec contract.--->Dec diastolic capacity---> Inc. diastolic press. - Hypoxia of myocytes - Myocardial loss from apoptosis and necrosis - Myocardial atrophy- - From injury, chronic wasting, starvation etc - Micro- - Myocytes look small - May contain lipofuscin- brown pigment |
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Non-lethal Myocardial degenerative changes
(x5) |
1) Fatty infiltration (NOT fatty change)- Inc lipocytes
- Due to obesity 2) Hydropic change- - Due to some drugs eg chemo agents - Tissue becomes grey, flabby and friable 3) Fatty change- abnormal retention of lipids - Due to systemic dz eg anaemia and bact. tox. - Not uniform throughout myocardium - Gross- pale, brown/yellow colour 4) Lipofuscinosis- Abnormal storage of lipofuscin - Aging change, except Ayrshire cows- hereditary - Gross- dark, brown/bronzed 5) Myocardial mineralisation- following necrosis |
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Myocardial necrosis
Causes- |
- Infectious- Distemper, Parvo, Blackleg, FMD
- Nutritional- Vit E/Selinium, Thiamine, Cu, K, Mg (-Vit E/ Sel= white mm dz (O+S), Mulb. heart dz (P)) - Toxic- Chemo agents- eg. doxorubicin, ionophores, thallium, cardiac glycosides - Neural- eg. - Brain-heart syndrome- infarct. in spinal cord (eg. RTA) ---> act. SNS ---> necrosis in heart - Circulatory- Ischaemia, embolism, thrombosis eg DIC |
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Necrosis-
Gross- Micro- Consequences- Sequence- |
- Gross- damage may not be seen <24hrs
- Palor c overlying fibrinonecrotic inflam. - Pale brown/ grey ---> white/yellow over time - Micro- - Necrotic myocytes- hypereosinophillic, striations lost, pyknotic nuclei - Consequence- mixed- No effect---> Death - Sequence- - Visable micro 6-12hrs later - >12hrs myocytes necrosis -24-48 hrs- MP + neut. infiltrate - Day 2-4- nec. becomes more prominant grossly - D 7-10- nec replaced by fibrosis + gran. tiss. - W.6- fibrosis well est., white scars +/- chalky mineral. |
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Inflammation of myocardium-
Causes- (x4) |
- Infectious- Parvo, Distemper, Picornavirus (P), FMD
- Bacteria- Blackleg, Listeriosis, caseous lymph., histophilus, any septicaemia - Protozoa- Toxoplasma gondii, neospora, - Parasites- cysticerca ovis, trichinella |
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Types of myocarditis-
(x6) |
- Suppurative- pyogenic bacteria- assoc c myocyte necrosis and abscess formation.
- Eosinophillic- parasites - Lymphocytic- viral (areas of palor) - Haemorrhagic- blackleg - Necrotizing- toxoplasma or acute viral infect. - (Pyo)granulomatous- chronic infect (+ neut.) eg FIP |
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Idiopathic cardiomyopathies-
(x3) |
- Hypertrophic
- Dilated - Restrictive |
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HCM
Describe- Gross- Micro- Presentation- |
- CATS
- Linked to a genetic malformation- Maine coons and holstein cattle - M > F, young- middle aged - Gross- Thickening of heart wall, Dec LV diam., LA dilat. - Micro- Myocyte disorg. and degen. c fibrosis - Dec. V compliance---> dec. diast. V filling - Presents as congestive heart failure, or... - Hind limb paresis due to "aortic saddle thrombosis" - Common cause of sudden death in Cats |
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DCM
Describe- Gross- Micro- Path- Presentation Variant- |
- DOGS (can occur in C,P)
- Large breed, middle aged, M > F dogs. Familial basis - Cats- due to taurine def.- rare - Gross- appears round, flabby c dil. of L/all chambers - Thickened, white endocardium and mild fibrosis. - Micro- Fibres NOT in disarray - Myocyte hypertrophy, atrophy, degen. and fibrosis -Path - may have valv. insuffic. - Dilation---> dec. contract.---> pump fail.---> dec CO - Present as chronic heart failure/ arrhythmia/ death - "Arrhythmogenic RV CM"- variant of DCM - replacement of myocyes in RV c fibrosis + fatty tissue |
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Restrictive-
Types- (x3) Describe- |
- Diffuse fibrosis of LV endothelium
- Thickened LV + LA dilation---> heart failure - Older male cats - Congenital endocardial fibroelastosis- cats - Excessive LV moderator bands |
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Myocardial circulatory disturbances-
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- Haemorrhage
- Thrombosis/ embolism and infarction - Rare in animals than people - Dz of coronary aa predisp. to thromb. eg. arterioscler. - Embolism may arise from L sided valv. endocarditis |
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Conduction system dz
(x4) |
- Sinoatrial conduction dist.- eg. hyperkalaemia
- AV block- 1st, 2nd, 3rd degree - Can occur due to scarring - 2nd degree block normal in fit horses - IntraV conduct. dist.- conduct. slowed or blocked - V pre-excitation- from access. conduct. pathways bypassing AV node |
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Cardiac neoplasia
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- Cardiac haemangiosarcoma- Common in GSD
- Usually effects RA - Gross- irregular, roughened dark red nodular masses - May be haem. into pericardial sac---> haemopericardium +/- cardiac tamponade - Metast. to lungs is common - Lymphoma- infiltration of neoplastic lymphocytes into myocardium in diffuse or focal/nodular pattern - Gross- White plaques/ nodules - Other - Heart base tumours from extra-cardiac tiss. eg. Chemodectoma (aorta) or ectopic thyroid tumour - Rhabdomyoma/myosarcoma - Myxoma- endocardium - Schwanoma- neurofibroma |
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Normal heart physiology-
Frank-Starling Mechanism- Hypertrophy- Neuroendocrine- Sympathetic activation RAA |
- F-S. mech.- Inc preload= Inc contractility
- HyperT- Inc Press---> Concentric / Inc Vol---> Eccentric - Symp. act.---> NA---> Inc VR, HR, contract., + vasoconstr. - RAA---> retention of Na+ and water + vasoconstr. - Renin from juxtaglomerulus app. - Angotensin 1--(ACE)--> 2---> stim Aldost. secretion - Endothelin-1---> Vasoconstrict. + Na+ retent. - ADH- water retention - Atrial natriuretic peptide- Dec Na+ uptake +H2O retent. |
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Heart Failure-
Forward Failure- Backwards Failure- Chronic Congestive heart failure- Acute- |
- Forward- fail. to maintain suff. CO to meet demand
- Back- Can only meet demands if filling press.> normal ---> Congestion behind heart - Chronic congest.- Insuff. CO to deal c VR---> congest. - Acute heart failure- - Severe cases eg. necrosis/ arrhythmia---> death - Less dire---> syncope--->comp. mech--->Inc HR, vasoC - Return to full funct. OR dec funct + reserve---> Chronic |
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Chronic Heart Failure
Systolic vs. Dyastolic |
- Chronic-
- Systolic- Dec. ejection of blood - Cause- - Impaired contractility e.g. DCM or myocardial infarct. - Valv. regurg. + chronic vol. overload eg. valvular endocardosis - Pressure overload (afterload) eg. subaortic stenosis or systemic hypertension - Dyasolic- impaired filling/ V relaxation -Cause- - Impaired relax- eg. HCM, RCM, myocardial fibrosis - Obstruct. to fill.- eg. AV valve stenosis due to valvular endocarditis |
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Left vs Right sided Cardiac failure
Cause- Effects- |
- Left
- Cause- Myocarditis, myocardial necrosis, CM, valve dz, any L--->R shunt - Backwards fail.---> Pulm. hypertens., congest., oedema, fibrosis - Forward fail.---> Dec CO--->Dec tiss. perf. ---> RAA syst activated ---> water retent.---> oedema ---> Hypox---> erythropoietin--->Inc RBC---> Inc PCV + viscosity ---> Dec renal perf.---> mild pre-renal azotaemia - Right- - Cause-Pulm hypertension, CM, myocarditis, valve dz, Cor Pulmonale. Often 2o to L due to Pulm hypertens. - Backwards failure---> Pass. congest., Inc venous press. ---> Spleno + Hepatomegaly ("nutmeg" liver) ---> Oed.- ascites (D), pleu. eff. (C), ventr. s/c oed. (H+R) ---> Dec. renal perf. ---> RAA---> Oedema + Azotaemia |
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Aneurysms-
Types Ruptures- Causes (x6) |
- Aneurysm- widening/ dilation of part of BV
- Mostly idiopathic - Thinning/ weaking of wall - Types- - Saccular, Berry, Fusiform, Dissecting - Dissect.- disrupt. to T.intima---> blood enters T. Med ---> splits BV wall - Rupture- Causes- - Trauma- eg. horse fall- Inc press.---> rupture ---> haemopericardium---> Cardiac tamponade---> shock - Spontaneous- eg. in turkey - Due to mycosis- eg. DAT - During parturition- uterine art. - Exercise induced - Other- Assoc. c Cu def., arteritis, breed- eg. greyhound |
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Growth disturbances-
Arterial hypertrophy- |
- Due to prolonged Inc press./ vol.
- Hypertrophy/plasia of T. media sm mm. - Pulm Art. hypertrophy - Causes- - Congenital shunting - Altitude - Parasites- Incidental finding after lung worm (C) |
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Degenerative conditions of BV
(x7) |
1) Arteriosclerosis
2) Atherosclerosis 3) Arterial medial calcification 4) Siderocalcinosis 5) Art. intimal calcif. 6) Fibrinoid necrosis 7) Vascular amyloidosis +hyaline degen. |
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Arteriosclerosis-
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- Hardening of artery
- Dev. c age - Idiopathic - Gross- White plaques - Micro- thickened T.intima, mucopolysacharride depo., fibrinisation, elastin degen. |
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Atherosclerosis-
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- Accum. of Fatty deposits and fibrous tiss. in BV wall---> narrowing
- Rare in animals- except in hyperthyroid induced hypercholesterolaemia. - Micro - Lipid droplets in myocytes - inc MP in T. media and intima |
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Arterial medial calcification
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- Granular Ca++ deposits- affect elastin of T. media
- Common - Pick up on radiograph - Causes- Chronic renal fail./ Vit D def/ Johnes/ spontaneous/ Toxins - Gross- Firm walls, crunchy texture, white plaques- may form complete ring |
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Siderocalcinosis
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- Ca and Fe deposits in cerebral art. of old horses
- incidental |
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Arterial initmal calcif.
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- "Intimal bodies"
- Small basophillic deposits on walls of small muscular arterioles in horses - Incidental |
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Fibrinoid necrosis
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- Due to endo damage---> fibrin form. and mural depos.
- Eosinophillic collar - Occurs in acute degen + inflam. (vasculitis) - May see 2o haem./ oedema - Eg.- Uraemia- renal failure (D) - Eg.- Selenium/ Vit E def.- mulberry heart dz (P) |
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Mulberry Heart Disease
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- Usually affects young, fast growing pigs (2-4 months)
- Found dead or if alive >24hr---> CNS changes - PM- Extensive haemorrhage, oedema, necrosis + fibrinous exudate. - May have thrombus formation. |
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Vascular Amyloidosis and hyaline degen.
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- Seen in small art. of spleen and heart
- Assoc. c areas of myocardial infarct. - Similar microscopic appearance to fibrinous necrosis - Eosinophillic areas - Differentiate with stains- - Amyloid- Congo red -Necrosis- PAS - Hyaline degeneration is negative for both |
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Thombosis/ Embolism
Predisposing factors- Thrombi- Gross appearance- |
- Virchow's triad-
- Vascular endothelial damage -eg. Infect., arteritis, fibrinoid necrosis, valvular endocarditis, Vit. E/ Selenium - Altered blood flow - eg. Turbulence- from defects, congestion/stasis- from chronic heart failure - Hypercoagulative states - eg. Renal dz, amyloid., DM, trauma, DIC, cancer, genetics - Thrombi- Gross- - Fast flowing aa- small, yellow/red-grey- line of Zahn - Slow- Red and gelatinous |
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Ischaemia and Infarction
Define- Changes- |
- Ischaemia- reduction in blood supply to a tissue
- Infarction- region of necrosis caused by peracute ischaemia - Wedge shaped - Red---> Pale over 1-5days (blood squeezed out by inflammation and lysed) - "Red zone"---> Granulation tiss. form. and MP infilt. |
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Inflammation
Define- Micro- Causes- |
- Vasculitis- inflam of BV
- Arteritis- inflam of arteries - Phlebitis- inflam of veins - Micro- - Perivasc. cuffing- leukocytes in and around walls - Necrosis of endo and sm mm cells - Fibrin depo. - Haemorrhage - Causes- - Infectious- - Viral- FIP, Equine viral arteritis, Bluetongue - Bacterial- Erysipelothrix, Salmonella, Histophilus - Fungal- Aspergillus - Parasotes- Dirofilaria, Angiostrongylus, S. Vulgaris - Immune-mediated disease- eg. Lupus, TIII HS - Extension of inflam. lesions from other tissue. |
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Neoplasia
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- Endothelial tumours-
- Haemangioma/ iosarcoma - Pleomorphic spindle shaped cells in bundles with collagenous CT - May or may not form blood filled vasc. channels - Can determine origin is vasc if stain for vWF (fact. XII) - Perivasc. wall tumours- spindle cells, different patterns - Haemangiopericytoma - Myopericytoma - Angiomyoma/sarcoma - Angiofibroma - Often locally invasive but rarely metastatic |
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Congenital dz of venous system-
|
- Portosystemic shunt- Portal v---> VC
- Portocaval shunt- Gastric- mesenteric v---> VC - Bypasses liver due to inc R - Intrahepatic vs extrahepatic vs both - Liver appears smaller (atrophic) and pale brown. |
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Plebitis
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- Cause-
- Systemic infection eg. Septicaemia - Local extension of infect. eg hepatic abscess - IV inject./ Catheter placement - Omphalophlebitis- Navel ill- inflam of umbilical v |
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Dz of lymphatics
Congenital- Inflam- Neoplasia- Other- |
- Congenital- Aplasia/ Hypoplasia---> lymphoedema
- Inflam- Lymphangitis - Causes- Bacteria -Johnes, TB, Actinobacillus, Glanders, Ulcerative lymph. (coryneb.), Epizootic lymph. (histoplasma) - Gross- Vessels are thicker, may ulcerate, lymphoedema, nodular suppurative lesions - Neoplasia- - Lymphangioma/ -angiosarcoma- rare and congenital - Gross- Often soft, poorly demarkated c clear exudate - Micro- Spindle shape, line collag. stroma, form clefts - Rupture- spontaneous/ traumatic---> chylothorax - Lymphangectasia- dilation of lymph.- often from inflam |
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Shock
Define- Types- (x5) |
- Hypoperfusion due to Dec CO or inadequate circ. vol.
---> Hyptoension---> Dec perf. + hypoxia - Types- - Cardiogenic- pump failure - Hypovolaemic- lack of circ vol. - Anaphylactic- Systm vasodil. + inc. perm assoc. c HS - Septic- Usually G-ve infect. - Neurogenic- loss of vasc. tone |
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DIC
Define- Sequence- (x5) Presentation- |
- Disseminated Intravascular Coagulation
- Thrombohaemorrhagic coagulopathy - 2o to range of dz eg. infect (G-ve), tiss. injury, neoplas. - Acute, subacute or chronic -Sequence 1) Release of tissue thromboplastic substances 2) Cause widespread injury to endothelium 3) 1+2---> Stim coag. pathway ---> Formation of microthrombi ---> Massive consumpt. of clotting factors ---> Activation of fibrinolytic pathways 4) Fibrin depo. ---> ischaem. + infarct. ---> Hypoxia ---> RBC haemolysis (due to trauma) 5) Haemorrhage due to lack of clotting factors - Presents as ischaemic tiss. damage or haem. |
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PM changes (and normal features)
(x9) |
1) Bones (ossa cordis) in aortic fibrous ring (O)- normal
2) Dilated lymphatics- white streaks- prominant on epicardial surface (H, O) 3) Haemoglobin imbibition- pink/red discol. of tiss. 4) Clots- absent in LV after rigor mortis due to contract. 5) "Chicken fat" clots- sedimentation of RBC pre-clotting 6) Cardiac haemorrhage 7) Rigor mortis- 1-6hrs after death, may last 24-48 hrs 8) Myocardial palor in young D+H---> normal histology 9) Intracard. euth ---> xll depos. on endo/epicardium --->Haem.---> pallor/ tan discol. + Haemopericardium |
